PT - JOURNAL ARTICLE AU - M. van der Stelt AU - W. B. Veldhuis AU - P. R. Bär AU - G. A. Veldink AU - J. F. G. Vliegenthart AU - K. Nicolay TI - Neuroprotection by Δ<sup>9</sup>-Tetrahydrocannabinol, the Main Active Compound in Marijuana, against Ouabain-Induced <em>In Vivo</em> Excitotoxicity AID - 10.1523/JNEUROSCI.21-17-06475.2001 DP - 2001 Sep 01 TA - The Journal of Neuroscience PG - 6475--6479 VI - 21 IP - 17 4099 - http://www.jneurosci.org/content/21/17/6475.short 4100 - http://www.jneurosci.org/content/21/17/6475.full SO - J. Neurosci.2001 Sep 01; 21 AB - Excitotoxicity is a paradigm used to explain the biochemical events in both acute neuronal damage and in slowly progressive, neurodegenerative diseases. Here, we show in a longitudinal magnetic resonance imaging study that Δ9-tetrahydrocannabinol (Δ9-THC), the main active compound in marijuana, reduces neuronal injury in neonatal rats injected intracerebrally with the Na+/K+-ATPase inhibitor ouabain to elicit excitotoxicity. In the acute phase Δ9-THC reduced the volume of cytotoxic edema by 22%. After 7 d, 36% less neuronal damage was observed in treated rats compared with control animals. Coadministration of the CB1 cannabinoid receptor antagonist SR141716 prevented the neuroprotective actions of Δ9-THC, indicating that Δ9-THC afforded protection to neurons via the CB1 receptor. In Δ9-THC-treated rats the volume of astrogliotic tissue was 36% smaller. The CB1 receptor antagonist did not block this effect. These results provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.